Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Total parenteral nutrition TPN has been used to treat or prevent malnutrition in 65 children with a variety of solid tumors and leukemia in the past 7 years. TPN was used in 58 patients with gastrointestinal complications of surgery, chemotherapy, or radiation; in 2 patients for preoperative correction of malnutrition; and in 8 who were entered into a prospective study. During TPN, general nutrition and appearance improved in all patients. Weight gain was noted in most. Despite gastrointestinal complications, which usually require the interruption of chemotherapy and radiation, treatment could be continued at full dose in 31 children with nutritional support by TPN. TPN was discontinued in 6 patients when blood cultures became positive. Sepsis was treated successfully by removal of the central venous catheter in all 6 and administration of antibiotics in 3. TPN appears to be safe and effective means of combating malnutrition which may occur with cancer and its therapy.
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PMID:Parenteral feeding in the management of children with cancer. 10 88

The effectiveness of enteral and parenteral feeding in supporting a satisfactory nutritional status and/or reversing protein-energy malnutrition was evaluated in 28 children, ages 1-19 (14 female) with advanced malignant disease (21 solid tumors, 7 leukemia-lymphoma). At the onset of treatment, 21 patients received intensive nutritional counseling (INC) and oral supplementation while seven received total parenteral nutrition (TPN). Sixteen of 21 patients who received INC had a decreased intake (x 48 +/- 24%) Recommended Dietary Allowances (RDA) for kilocalories and dramatic weight loss (x 16.4 +/- 12.4%). A total of 18 patients received TPN for a mean of 24 days (7-60); kcal averaged 90 +/- 26% RDA during weight gain. At onset of TPN, the mean serum albumin, transferrin and total lymphocyte counts were 3.06 +/- 0.38 g/dl, 175 +/- 62 mg/dl, and 1102 +/- 966/mm3 respectively, 15/18 children had subnormal anthropometric measurements and 17/18 patients were anergic to recall skin test antigens. TPN for less than 9-14 days neither repleted weight, skinfold reserves, nor serum albumin concentrations (greater than 3.2 g/dl) although an early increase (p less than .02) in transferrin concentration was observed. However, TPN for 28 days supported weight gain (3.27 kg, 16 +/- 6%), increased serum albumin (0.62 +/- 0.43 g/dl, p less than .001) and transferrin (62 +/- 42, p less than .002) to normal concentrations and reversed anergy in 7/11 patients retested. This study documents the severity of protein energy malnutrition which accompanies intense treatment of children with cancer and the nutritional and immunological benefits of a 28 day course of TPN.
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PMID:Reversal of protein-energy malnutrition in children during treatment of advanced neoplastic disease. 22 80

Electrolyte disturbances in leukemia can be the result of the disease process or drug therapy. One group of electrolyte abnormalities is related to the stage of the leukemic process. Included in this group are newly diagnosed patients who may show elevated serum potassium, phosphorus, and magnesium--a result of their release from malignant cells after cytotoxic therapy or their accumulation due to urate nephropathy. Patients in remission usually have normal serum electrolyte concentrations, but acute leukemia patients during relapse may have hypokalemia, hypophosphatemia, and hypomagnesemia. This imbalance may be related to cellular uptake of these electrolytes in the presence of inadequate dietary intake. Other factors contributing to electrolyte derangements, and related to the leukemic process, include hyponatremia and hypochloremia secondary to the SIADH, hypokalemia in acute monocytic or acute myelomonocytic leukemia due to lysozyme-induced tubular damage, hypercalcemia possibly secondary to leukemic infiltration of bone or parathyroid glands (with PTH release), or production of a PTH-like substance by leukemic cells. Nonspecific factors related to the disease process which may aggravate the electrolyte imbalance include gastrointestinal loss through nausea, vomiting, and malnutrition. The drug-related electrolyte abnormalities include cyclophosphamide- and vincristine-induced SIADH; decreased serum sodium, chloride, potassium, and calcium concentrations as a result of polymyxin B nephrotoxicity; hypokalemia and hypomagnesemia secondary to amphotericin B; hypocalcemia, hypophosphatemia, and hyperphosphaturia due to L-asparaginase-induced hypoparathyroidism; hypokalemia due to a nonreabsorbable anion effect of antibiotics in the distal tubule or changes in membrane ionic transport of all cells by large doses of antibiotics. Electrolyte disturbance in leukemia thus have a multifactorial pathogenesis which can best be delineated according to the stage of the leukemic process and the drugs being used. Recognition of the cause or causes in a particular patient is essential for an effective approach to management. This review emphasizes the need for routine measurement of serum electrolytes during all phases of the leukemic process.
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PMID:Electrolyte and acid-base disturbances in the management of leukemia. 26 90

A study of 3451 cholesterol determinations in different diseases was carried out. The mean cholesterol levels for male and female adults and children with different diseases were compared with values for their healthy counterparts. Sickle cell anemia, leukemia, liver cirrhosis, hepatosplenomegaly, tuberculosis, and diabetic, nutritional, ataxic, and tropical neuropathies in male and female adults were associated with reduced cholesterol level while in children malnutrition and anemia were the main causes of low cholesterol levels. Obesity and hypertension caused an elevated level but the mean values were within the range for adult Nigerians in the high income group. Only nephrotic syndrome in both adult and children was associated with a markedly increased cholesterol level in Nigerians of low income status.
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PMID:Serum cholesterol and diseases in Nigerians. 50 76

A nine years old female child with malnutrition who showed, six months before admission, a number of clinical manifestations consistent with leukemia. The outstanding clinical manifestation during her hospital stay was that of pericarditis with effusion, which was found associated with pericardial leukemic infiltration. The final picture was that of cardiorespiratory failure associated, both to leukemic infiltration of these organs, as to that of postoperative hemorrhage.
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PMID:[Acute leukemia with cardiac infiltration]. 125 21

Retrovirus infection, cocaine administration, and nutritional deficiencies are known to individually produce impairment of the immune system. Therefore, we developed a murine model to study the effect of daily cocaine administration, protein malnutrition, and retrovirus infection causing murine AIDS on the lymphoid cell populations of the thymus. C57BL/6 female mice fed a diet containing 4% protein were studied following chronic cocaine administration and LP-BM5 murine leukemia virus (MuLV) infection. Cocaine administration reduced body and thymus weight. Cocaine partially prevented thymus enlargement due to lymphoid cell proliferation induced by murine retrovirus infection. Cocaine treatment affected dramatically the thymus of protein-malnourished mice where the absolute number of Thy 1.2+, CD4+ and CD8+ cells represented only 10% of the control values. Daily saline injection also induced a significant decrease in the number of Thy 1.2+, CD4+ and CD8+ cells per thymus. These results suggest that the thymus glands of mice fed a low protein diet were susceptible to stress. Retrovirus infection provoked a decrease in the percentage and absolute number of Thy 1.2+, CD4+ and CD8+ cells in the thymus. This effect was potentiated by cocaine treatment. Therefore, cocaine was able to potentiate the impairment of the immune system caused by MuLV infection. We consider that cocaine could alter the immune system by altering the expression of T cell differentiation markers after direct interaction with thymocytes or through the neuroendocrine-thymus axis. Moreover, this effect was more dramatic and severe during protein malnutrition.
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PMID:Alteration of thymic cell subsets by cocaine administration and murine retrovirus infection in protein undernourished mice. 133 87

Bacterial translocation is defined as the passage of viable bacteria from the gastrointestinal tract to extraintestinal sites, such as the mesenteric lymph node complex, liver, spleen, kidney, and blood. The major mechanisms promoting bacterial translocation in animal models are: (a) disruption of the ecologic equilibrium to allow intestinal bacterial overgrowth, (b) deficiencies in host immune defenses, and (c) increased permeability of the intestinal mucosal barrier. These mechanisms can act in concert to promote synergistically the systemic spread of indigenous translocating bacteria to cause lethal sepsis. Studies are presented of attempts to delineate the mechanisms promoting bacterial translocation utilizing animal models of intestinal bacterial overgrowth, immunosuppression, T-cell deficiencies, solid tumors, leukemia, diabetes, endotoxemia, hemorrhagic shock, thermal injury, bowel obstruction, bile duct ligation, protein malnutrition and parenteral nutrition. Also described are the use of selective antibiotic decontamination or nonspecific macrophage immunomodulators in attempts to reduce bacterial translocation from the gastrointestinal tract.
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PMID:Bacterial translocation from the gastrointestinal tract. 147 1

Cancrum oris is predominantly seen in children in underdeveloped countries where widespread malnutrition, dehydration and epidemic infections are present. In the western world, it is sometimes found in immunosuppressed adults with predisposing conditions such as leukaemia and infection associated with malnutrition. Early diagnosis and an intensive therapeutic approach are the key to a favourable prognosis of noma-like necro-ulcerative lesions. The prognosis is significantly improved if the predisposing condition can be removed. Two cases are presented and the treatment is discussed.
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PMID:Cancrum oris-like lesions. 162 72

Humoral immunity involves molecules in solution in biological fluids including effectors of non specific immunity (e.g. complement, cytokines) and specific immunity (antibodies) as well. Acquired humoral immunodeficiences are often multifactorial in origin and associated with defects of cell-mediated immunity. The most common etiologies are those of iatrogenic immunodeficiencies: surgery (especially splenectomy), radiotherapy, chemotherapy of leukemia and cancer, immunosuppressive treatments in organ transplanted patients. Protein-caloric malnutrition also induces cellular and humoral immunodeficiencies. Among other causes, three types of diseases may induce defective antibody production: 1/B cell neoplasias (e.g. multiple myeloma, chronic lymphocytic leukemia...) 2/renal diseases (nephrotic syndrome, renal insufficiency) and 3/various infectious diseases, including AIDS. Some principles of prevention and treatment of secondary humoral immunodeficiencies are given.
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PMID:[Secondary deficiencies of humoral immunity]. 204 15

Deficiency of the purine metabolic enzyme adenosine deaminase causes severe immunodeficiency. Retroviruses have been reported to decrease the activity of adenosine deaminase, and many retroviruses, including feline leukemia virus, cause immunodeficiency. Levels of purine metabolic enzymes including adenosine deaminase and consequences of adenosine deaminase inhibition were investigated in feline leukemia virus-infected fresh tumor cells and infected and uninfected cell lines. No evidence of virus effect on levels of adenosine deaminase or other purine metabolic enzymes was detected. Neoplastic cells demonstrated considerable heterogeneity of activity levels of purine metabolic enzymes.
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PMID:Purine metabolism in feline lymphomas. 216 Nov 36


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